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In this study, Trf1 genetic deletion in mice, including those with cancer-prone mutations, was shown to not affect overall viability and cause only mild effects, while being necessary for tumor formation, suggesting a potential therapeutic window for Trf1 as an anti-cancer target.

This study found that abolishing H3K27me3 in mouse skin by targeting Ezh2 and Ezh1 affects hair follicle development and epidermal behavior, revealing functional differences between these tissues.

This review discusses genome maintenance mechanisms critical for preventing age-related diseases by preserving stem and progenitor cell potential, but reports no new empirical findings.

This review discusses the senescence–stemness connection in cellular biology and reports no new findings, highlighting implications for both tissue repair and aggressive cancer behavior.

This workshop review discusses the dual role of cellular senescence in cancer, highlighting both its anticancer effects and pro-tumorigenic potential, while reporting no new research results.

This review discusses the regulation and dynamics of the Wnt/β-catenin signaling pathway in development, pluripotency, and cancer, highlighting potential mechanisms and future research directions, but reports no new results.

Histone demethylases play a key role in the development of many diseases and may be targets for treatment.

p14ARF and p16Ink4a cause hair follicle stem cell aging and dysfunction.

This study found that mice lacking the Sept4/ARTS gene had more hair follicle stem cells and improved wound healing, suggesting apoptosis regulation as a potential target in regenerative medicine.

In this study, inactivating the TAF4 subunit of transcription factor TFIID in mouse epidermis disrupted gene expression linked to skin and hair function, and increased tumor risk.

In this study, deletion of ROBO4 in mice ameliorated hair loss caused by elevated PAF levels, suggesting potential interplay with VLDLR-related pathways.

Ivarmacitinib effectively regrows hair in severe alopecia areata.

This study shows that IKZF1 and the protein IKAROS may play a role in the development of alopecia areata, based on findings from both mouse models and human scalp tissues.

In this mouse model study, researchers observed that RIPK1 inhibitors delayed the onset of alopecia areata by modulating immune cells, specifically dendritic and CD8+ T cells, and increased hair length in organ culture mimicking the condition.

In a mouse model study, researchers found that mutations in Aire reduced alopecia areata frequency, while Notch4 mutations did not lead to the disease, likely due to proximity with a resistance gene.

In this study, deleting the Igf1 receptor in specific skin cells of mice affected hair follicle cycling but not overall skin health, suggesting Igf1r's role in hair cycle regulation through Bmp-4 activation.

This study concluded that KLF4 is a crucial regulator of hair follicle stem cell quiescence and may work by interacting with multiple transcription factors to control related genes.

This study identified a new keratin, K6irs, as a potential histological marker for the inner root sheath of hair follicles in mice and humans, and as a candidate gene for hereditary hair defects.

In this study using a mouse model, RIPK1 inhibitors were found to delay the onset of alopecia areata, reduce immune cell numbers in affected skin, and increase hair length, indicating a potential therapeutic role in preventing alopecia areata.

This study found that the DKK3-CKAP4 signaling axis is involved in fibroimmune remodeling in androgenetic alopecia and that targeting this pathway may restore a regenerative hair follicle environment, offering a potential therapeutic strategy to counteract hair follicle miniaturization.

This study found that selective deletion of PIKFyve kinase using a PF4 promoter in mice led to defective platelet lysosome biogenesis and a prothrombotic effect, with unexpected macrophage infiltration in multiple organs.

This study reported that Dkk4-knockout mice showed disrupted hair follicle patterning, suggesting a WNT-DKK axis may influence regional specificities in hair follicle induction related to androgenetic alopecia.

A missing mK6irs1 gene causes hair loss in mice.

This study found that Dkk4-knockout mice exhibited disrupted hair follicle patterning, including a lack of the first wave of hair follicles in the lateral back skin.

This study found that ACKR2 plays a crucial role in reducing inflammatory skin fibrosis and promoting inflammation resolution through IFN‐β production, limiting tissue scarring.

This research developed new in vitro models for high-throughput screening of drugs that could protect or restore immune privilege in hair follicles, finding that Tofacitinib was effective in preventing inflammation-related marker upregulation, while Tacrolimus and αMSH worked specifically in outer root sheath keratinocytes.

ITK inhibitors may effectively treat alopecia areata.

In this study, the pi4kβ1β2 double mutant in Arabidopsis thaliana exhibited altered root growth, increased susceptibility to Blumeria graminis, and a potential correlation between PI4K activity and auxin response and immunity due to changes in vesicular trafficking and actin filaments.

This study found that overexpression and knockdown of DKK4 influence genes involved in hair follicle growth and development in Angora rabbits and identified specific SNPs in DKK4 associated with wool quality, notably showing that the TT/GG haplotype combination relates to higher fibre diameters.